Hepatitis A causes one of the most common infectious diseases in the world and may produce clinical conditions ranging from asymptomatic infection to acute liver failure. Koff reviews the role of immunization in the prevention of this disease.

The RNA virus responsible for hepatitis A is a small, non-enveloped, spherical particle that is thermostable and acid-resistant. The liver is the only target organ, but little is understood about the minimum infective dose, gastrointestinal transport mechanisms or receptors in the liver that facilitate infection. Virus replication takes place exclusively in infected hepatocytes, and viral particles then pass through the biliary system into the intestine to continue the cycle of fecal-oral infection in another host. Hepatitis A virus is excreted in the feces for up to two weeks before symptoms appear, reaching a peak at the onset of symptoms and continuing for at least another week. Viral shedding declines rapidly but may continue for several months in a few persons. The average incubation period is 30 days (range: 15 to 50 days). About one third of the U.S. population has serologic evidence of previous infection, but this rate is declining, presumably as a result of improved hygiene. Person-to-person transmission within the household is the most common mode of infection, but community outbreaks also occur because of contamination of water or food.

Patients with hepatitis A infection may have any combination of gastrointestinal and systemic complaints such as fever, malaise, weakness, anorexia, arthralgias, myalgia and flu-like symptoms. Jaundice with dark urine, pruritus and hepatic tenderness may occur. Serum aminotransferase levels are usually elevated, and IgM antibody is detectable for three to six months after infection. Bilirubin concentrations are elevated in patients with jaundice. Most patients recover spontaneously with symptomatic treatment and complete abstinence from alcohol. Patients rarely develop relapsing hepatitis, cholestatic hepatitis or acute liver failure requiring transplantation.

The traditional preventive measure for hepatitis A infection is passive immunization with immunoglobulin containing IgG antibody to hepatitis A virus. This measure is still recommended for children younger than two years and for postexposure prophylaxis of household contacts of infected persons. Immunoglobulin may not be effective if given more than two weeks after exposure; protection lasts for no more than six months. Live attenuated hepatitis A vaccines are being developed in China, and several inactivated vaccines are available in Europe and the United States. These inactivated vaccines produce antibody levels comparable to those achieved following natural infection and approximately 15 times those attained by passive immunization. Studies indicate that most recipients seroconvert, with the exception of very young children, who may have a blunted response because of maternal antibodies. Projections indicate immunity from hepatitis A virus lasts for at least 10 years after two doses of vaccine.

The author concludes that education and immunization are vital to controlling hepatitis A infection. Travelers should be vaccinated for hepatitis A virus two weeks before travel to endemic areas. Immunoglobulin may also be administered at the time of vaccination, at a separate site, if travel is to occur in less than two weeks. Vaccination is also recommended for persons who are at high risk of fecal-oral spread because of sexual practices or poor hygiene, and for persons whose professions put them at high risk—sewage workers, health and child care workers, and veterinary surgeons. In developed countries, good hygiene is likely to be a major factor in controlling hepatitis A. In developing countries, universal vaccination in childhood is the optimal strategy and may become possible when vaccines for hepatitis A are made available in a combined form with other “routine” immunizations.